Exam II :0 Flashcards
(156 cards)
1
Q
What are the two neurons in an autonomic chain called?
A
The preganglionic neutron, and the post-ganglionic neuron
2
Q
Where the preganglionic cell bodies are located in the CNS
A
Sympathetic region- the thoracolumbar region (T1,L2,L3)
Parasympathetic- the craniosacral regions (S2–S4, and the brainstem)
3
Q
The axon lengths of the preganglionic and postganglionic neurons.
A
Sympathetic preganglionic- short
Sympathetic postganglionic- long
Parasympathetic preganglionic- long
Parasympathetic postganglionic- short
4
Q
What neurotransmitter is released by the preganglionic neurons of the sympathetic and parasympathetic nervous systems?
A
The neurotransmitter for both is Acetylcholine (ACh)
5
Q
The receptors that are located on the postganglionic neurons.
A
The receptor for both is the nicotinic acetylcholine receptor
6
Q
The neurotransmitter that is released by the postganglionic neurons.
A
Sympathetic- Norepinephrine
Parasympathetic- Acetylcholine (ACh)
7
Q
Compare/contrast the sympathetic and parasympathetic divisions of the ANS in terms of:
The receptors that are located on the effector/target organs.
A
Sympathetic- Adrenergic (alpha, beta)
Parasympathetic- Muscarinic acetylcholine receptors
8
Q
sympathetic nervous system known as the what?
A
fight or flight, maintains homesostasis in times of crisis
9
Q
The parasympathetic-
A
basically to ensure relaxation
10
Q
What is the name of the neuron that leaves the brain stem/spinal chord for sympathetic and parasympathetic nervous systems?
A
pre-ganglionic neurons,
next is post-ganglionic neuron
11
Q
What is a ganlion?
A
cell body is almost or outside of the central nervous system
12
Q
Sympathetic region-
A
the thoracolumbar region (T1,L2,L3)
13
Q
Parasympathetic regions-
A
the craniosacral regions (S2–S4, and the brainstem)
14
Q
Describe the axon lengths of the sympathetic nervous system
A
Preganglionic- short
Postganglionic- long
15
Q
Describe the axon lengths of the parasympathetic nervous system
A
Preganglionic- long
Postganglionic- short
16
Q
The synpathetic nervous systems ganglia are close to the
A
spinal chord
17
Q
Activing one of sympathetic nervous system means-
A
you activate it all
18
Q
In order for acetyl choline to stimulate the post-ganglionic neuron (after being preleased by the pre) what receptor?
A
Nicotinic receptors (para and sym)
19
Q
What is the effector in terms of the autonomic nervous system?
A
the target organ or tissue
20
Q
What are some examples of functions of the parasym nervous system?
A
-salivation
-pupil constriction
-bladder contraction to pee
-
21
Q
What neurotransmitter is emitted from the post-ganglionic neurons in the parasym nervous system?
(bonus for receptor type)
A
Acetylcholine bb
receptor here will be muscarinic
22
Q
What is the receptor at the effector for the parasym nervous system?
A
Muscarinic
23
Q
Some examples of sym responses?
A
-heart rate increase
-release of adrenaline by adrenal gland into bloodstream
-every target organ with sympathetic will then be activated
-relaxes bladder
24
Q
What neurotransmitter is emitted from the post-ganglionic neurons in the sym nervous system?
(bonus for receptor type)
A
Norepinephrine
Adrenergic receptors
25
What is the receptor at the effector for the sym nervous system?
Adrenergic receptors
26
Main differences between:
Autonomic nervous system
Core nervous system (central nervous system)
Autonomic nervous system- compare and contrast sympathetic and parasympathetic
Core nervous system central nervous system (brain and spinal chord) intaking sensory info, making response
27
General info about autonomic nervous system
Efferent is a autonomic pathways, involuntary control, smooth muscle, cardiac muscle, glands
28
In autonomic nervous system, where the ganglions at?
Preganglionic- cell bodies in central nervous system
Postsynaptic- cell bodies in autonomic nervous system
29
What is a ganglion?
cluster of cell bodies in peripheral nervous system
30
-2 synapses, where located?
one between pre and post, and one between post and target or effector organs
(axons will leave and go into peripheral nervous system)
31
What is the significance of divergence & varicosities in the autonomic nervous sytsem?
(pp 06 slide 6)
Divergence allows for coordination of multiple organs
-varicosities allow coordination of all the cells in a single organ (axon terminal elongated with sweelings, at each swelling can release neurotransmitter)
32
Do divergence and varicosities allow for autonomic nervous to have fine control?
NO -these don’t allow for fine control, that’s not autonomic nervous system
33
What are Chromaffin cells?
-modified *sympathetic postganglionic cells* of sympathetic branch
(not neurons, *endocrine cells* that release epinephrin/norepeiephrin into the blood)
34
Where are Chromaffin cells found in mammals?
Found in the adrenal medulla in mammals
(various locations in other verts)
35
Sympathetic postganglionic cells vs chromaffin cells
-have more localized control, with through adrenal medulla dumped in blood, not specified
-epinephrine in blood good, change everyone all at once
-adrenal medulla for massive rapid response.
36
Cardiovascular:
Sympathetic- Higher heart rate, higher BP, vasoconstriction
Parasympathetic- Lower heart rate, lower BP, vasodilation
37
Respiratory:
Sympathetic- dilation, increased breathing rate, less mucus
Parasympathetic- constriction, lower breathing rate, more mucus
38
Digestive:
Sympathetic- less motility, less secretions, higher sphincter tone
Parasympathetic- more motility, more secretions, lower sphincter tone
39
Urinary:
Sympathetic- Less urination, bladder relaxed, sphincter contracted
Parasympathetic- more urination, bladder contracted, sphincter relaxed
40
Antagonistic control (via sympathetic and parasympathetic)
Pacemaker cells of heart get input from both, para decrease, sympa increase
-At rest both branches are active to a small degree
41
Tonic control (input from one branch or another)
raising or lowering amount of sympathetic input (from one branch really)
42
Does sym or parasym usually control blood vessel dilation?
-blood vessels usually sympathetic input (tonic instead of antagonistic)
-if want broaden decrease baseline sympathetic input to loosen the blood vessels
43
Tonic vs Antagonistic control-
-Tonic control is a continuous regulatory mechanism
-Antagonistic control uses opposing regulators to control a function.
44
a-receptor response:
what happen?
-epinephrine + a-receptor, vessel contracts
-a-receptors usually digestive, b-receptors more to muscles (think of flee)
45
beta receptor response:
Epinephrine + beta-receptor, vessel dilates
46
Why big dump of epinephrine very helpful if need to fight or flight?
-If chroma? cells activated, dump of epinephrine in body
-widespread redistribution of blood from what is not needed to what is really needed
47
What is the difference between endocrine and exocrine?
The endocrine system regulates the internal environment, and releases hormones into
the bloodstream.
The exocrine system will secretes hormones into ducts to go to some external location
48
What are the three main differences between the endocrine and nervous systems?
Endo-
1) Can reach over long distances across the body, very widespread
2) The system reacts slowly since the hormones are pumped into into the blood
3) May still have stimulation after the hormones have stopped being sent
49
What is the difference between endocrine, paracrine, and autocrine?
Endocrine- hormones that go over long distances in the body through the blood
Paracrine- target cells that are nearby
Autocrine- signals from a cell to itself
50
What is a hormone?
A hormone is a chemical messenger triggering a specific effect in a target cell.
51
What are the three categories of hormones and where are the receptors that each binds to?
1) Peptides (protein hormones, water soluble, and interact with receptors on the cell surface, example
insulin)
2) Steriods (lipid soluble hormones) react with receptor sites inside the cell (example testosterone)
3) Amines (amino acid derivitvies) configuration will change how they interact, could be cell surface or
cell interior receptor
52
Peptide hormones, what are there general properties, and what receptors do they bind?
-Protein hormones, water soluble,
-interact with receptors on the cell surface, example
insulin)
53
Steroids, what are there general properties, and what receptors do they bind?
(lipid soluble hormones)
-react with receptor sites inside the cell (example testosterone)
54
Amines , what are there general properties, and what receptors do they bind?
(amino acid derivatives)
-configuration will change how they interact, could be cell surface or cell interior receptor
55
Classical definition of hormones-
-secreted into the blood by cells or glands
-act on long distance targets
-active at very low concentration
-no matter what the tissue is, it’ll release a hormone
56
What are some criteria a hormone must meet?
must be secreted into blood, can have effect very far away from point of release.
Typically cells are very sensitive, don’t need high concentrations of hormones
57
Mechanisms of action (hormones)-
(.)(.) boobs hehe
-change enzymatic reaction rate by modifying proteins
-can affect membrane transport, adding or removing to change who can go in or out of cell (can occur pretty quickly)
-alter gene expression, turn on or off (slower process)
58
Main difference between neurotransmitters and hormones?
-neurotransmitters have effect while being released, some hormones like that, but some take long time to take action
59
What mainly determines hormone concentrations?
-Negative-feedback (multi-step process) maintains stable plasma concentration, good way to make sure hormone concentrations don’t change that much
-Neuroendocrine reflexes, rapidly increases plasma concentration in response to stimulus. Big increases with stimulus and then big decreases when not
-Rhythmic release- plasma concentration fluctuates over time, regular changes, (example could be melatonin with darkness)
60
Role of receptors-
Cells only respond if they have the right receptor
-changes in receptor number affect sensitivity
61
How do cells manage receptors?
Up-regulation: adding receptors
Down-regulation: removing receptors
-can happen in endocrine systems
-uncommon for target tissue to be exposed to one hormone at a time, some interact with each other
62
Hormones are spatially nonselective, but
usually have target tissues
63
Categories of Hormone Interaction-
-Synergism (combo causes bigger jump, all have similar effect, combined get amplification of massive effect)
-Permissiveness (one on it’s own will have no effect, need 2 together to get big payout. One has the effect, the other permits the other to do its job)
-Antagonism (two hormones that send physiological variable in opposite directions) often at least 2 hormones that can do this, an example is blood glucose, insulin, and glucagon. **see slides and video ~21 minutes to review that mechanism
64
Synergism (of hormones)
combo causes bigger jump, all have similar effect, combined get amplification of massive effect
65
Permissiveness (of hormones)
-one on its own will have no effect, need 2 together to get big payout. One has the effect, the other permits the other to do its job
66
Antagonism (of hormones)
(two hormones that send physiological variable in opposite directions)
often at least 2 hormones that can do this, an example is blood glucose, insulin, and glucagon.
67
**see slides and video (2-5-25) ~21 minutes to review that mechanism
07 slide 9
68
The pituitary gland-
“neuro endocrine system”
-base of gland, in us around pea sized. Physically connected to hypothalamus through pituitary stock
-Pituitary has anterior and posterior
69
Posterior pituitary-
-2 different sets of hypothalamic neurons involved in hormone release from posterior pituitary
Releases 2 neurohormones, vasopressin (vasotocin for non-mammals) and Oxytocin (mesotocin for non-mammals)
69
Anterior Pituitary-
(a little more complex😩)
Hypothalamic-hypophyseal portal system
Hypothalamic neurohormones released into portal system (Tropic hormones)
Anterior pituitary hormones: released into general circulation
-peripheral targets release their hormones
69
-Pituitary has anterior and posterior
What tissue composes each?
Anterior-glandular tissue
Posterior- neural tissue like rest of brain
Release of hormones from each different
70
How are hormones released from the posterior pituitary?
Sequence of events-
Made in hypothalamic neurons
-released in posterior pituitary
-distributed to body via blood
Capillary bed specialized for release I think
-Neurons in hypothalamus, pituitary stock mainly axons
71
Hormones released by the anterior pituitary-
1) prolactin (usually not tropic, direct effects)
2) growth hormone (usually not tropic, direct effects)
3) Follicle stimulating hormone (FSH)
4) Luteinizing hormone (LH)
5) Thyroid-stimulating hormone (TSH)
6) Adrenocorticotopic hormone (ACTH)
72
Pituitary feedback loops-
-hormones (not physiological response) are involved in negative feedback
-Patterns of hormone levels can help identify location of secretion imbalances
-need to identify where in pathway youre having problem if someone has hormone imbalance
-Hyposecretion vs hypersecretion
-primary vs secondary pathology
73
Upregulating & downregulation of receptors can partially counteract
imbalances
74
Negative feedback provides clues to
location where endocrine is goin wrong
75
Tropic hormones don’t have a direct effect on
target tissue
76
Generalized hypothalamic-hypophyseal pathway regulating the release of hormones from
peripheral endocrine glands
(do see screenshot)
Hypothalamus
Tropic hormone 1
Anterior pituitary gland
Tropic hormone 2
Peripheral gland
Peripheral hormone
Non-endocrine target
77
Put the following in order from largest to smallest: myofibril, myofilament, muscle fiber, muscle,
sarcomere, fascicle
Muscle, Fascicle, Muscle Fiber, Myofibril, Sarcomere, Myofilament
78
What is the sarcolemma?
The plasma membrane of a muscle cell that surrounds the cell and helps trigger action potentials (which will allow for muscle contractions.)
79
Which proteins are found in thick filaments?
Thick- myosin
80
Which proteins are found in the thin filaments?
Thin- actin
(also elastic filaments made of titin)
81
Briefly describe the sliding filament model of muscle contraction
When stimulated, the myosin heads will interact with the binding sites of the actin subunits.
The attachments will break and form, pulling the z disks toward the m line.
Adjacent A bands will get closer and closer causing contraction.
82
What is the synapse between a motor neuron and a muscle fiber called?
The neuromuscular junction
83
Which neurotransmitter is released by motor neurons?
Acetylcholine
84
Which ion is released into the muscle fiber when an action potential spreads down the t-tubules?
Ca2+ ions
85
What change happens in the thin filaments that allows myosin to bind to actin?
Calcium will bind to troponin, which frees the actin to bind with the myosin.
86
Muscle –
The entire muscle (e.g., biceps) is made up of bundles of fascicles.
87
Fascicle –
A bundle of muscle fibers (cells) wrapped in connective tissue.
88
Muscle fiber (muscle cell) –
A single elongated multinucleated muscle cell.
89
Myofibril –
Long, thread-like structures inside muscle fibers, composed of repeating units called sarcomeres.
90
Sarcomere –
The functional contractile unit of a myofibril, consisting of thick and thin myofilaments
91
Myofilament –
The smallest structural components, including actin (thin filaments) and myosin (thick filaments), which slide past each other during contraction.
92
Entire muscle fiber will contract, and then if enough contract
then the whole muscle will contract
92
Describes myofibril element organization
-don’t have a single row of thin filaments but 2 rows, one on either side of the sarcomere, alternating thich thin thich thin
-2 ends start apart (of sarcomere) then grab and tug
93
Thick filaments:
How many proteins comprise, what are?
myosin molecules
Tail, hinge region, head (aka cross bridge)
2 special regions on myosin head-
-Actin binding site
-Myosin ATPase site ** consult diagram ATPase hydrolyzes ATP and powers muscle contraction
94
Thin filaments-
How many proteins comprise?
What are?
more complex composed of 3 proteins-
Actin molecules: form actin helix (2 strings of beads twisted together_, myosin binding site
Tropomyosin: Threadlike protein wrapped around actin helix, nothing binds to it
Troponin: globular protein that is bound to tropomyosin (packed on,) Ca2+ binding site
95
Actin molecules:
(thin filaments)
form actin helix (2 strings of beads twisted together_, myosin binding site
96
Tropomyosin:
(thin filaments)
Threadlike protein wrapped around actin helix, nothing binds to it
97
Troponin:
(thin filaments)
globular protein that is bound to tropomyosin (packed on,) Ca2+ binding site
98
2 special regions on myosin head-
-Actin binding site
-Myosin ATPase site ** consult diagram ATPase hydrolyzes ATP and powers muscle contraction 08 slide 5
99
-first stage at neuromuscular junction, then excitation of muscle fiber (electrically excitable tissues, can fire action potentials, after firing there will be an influx of calcium into the cell which will lead to contraction relaxation.)
-sliding filament mechanism, cross which cycle, excitation and action coupling last 3 things that happen I think, muscle fiber fire action potential, will contract, calcium brings them together
100
Neuromuscular junction-
-acetylcholine released by motor neuron
-Nicotinic ACh receptors on muscle fiber (permeable to both Na+ and K+)
-action potential spreads down causing calcium to rush in, vesicles open, ACh will diffuse out and find Nicotinic ACh receptors on muscle fiber
-these channels permeable to Na+a nd K+, when they open up the flow across muscle fiber membrane will change
101
What will happen to the membrane potential when nAChRs open and why?
Permeability to both Na+ and K+ will increase, but we would expect depolarization of the membrane potential. This is because sodium will be entering the cell faster than K+ will leave the cell. This is because the electrochemical gradient is stronger for Na+ going into the cell than the one acting on K+.
102
Neuromuscular junction-
-Acetylchline is released by motor neuron
-Nicotinic ACh receptors on muscle fiber
-Acetylcholine broken down by acetylcholinesterase (allow for rapid degradation so muscle contraction will stop immediately, allows for fine-tuning of muscle action)
103
Action potential Generation-
-graded potential triggers action potential
-Action potential spreads across sarcolemma (membrane of muscle fiber, cell membrane) & down t-tubules (tunnels that burrow deep into muscle fiber, (little perforations lead to t-tubule) when action potential is spreading down membrane, also heads down t-tubules into muscle
104
Where will an action potential begin in a muscle fiber?
-action potential begins in middle of muscle fiber
105
T-tubules positioning corresponds
to where 2 sarcomeres meet
106
Every end of sarcomere has
t-tubule
107
What's even the point of them t-tubules?
Change in membrane potential only happens at surface of membrane, electrode in middle of cell wouldn’t catch change
-reason for t-tubules is to carry charge deep into middle of muscle fiber, myofibrils and sarcomeres are deep inside as well, and all of them need to be hit by the action potentials that are firing. Will lead to increase in amount of calcium inside cell
108
Action potential triggers Ca2+ release from
Sarcoplasmic reticulum (not endoplasmic bc idk)
-The SR sequesters calcium, lots in this organelle relative to ICFluid
109
When muscle fiber fires action potential down t tubules, calcium in SR released into intracelluarfluid, this happens through 2 proteins:
-dihydropyridine (DHP) receptor- located in membrane of t-tubule (not an ion channel, receptor voltage sensitive protein)
-Ryanodine receptor (RyR)- in SR membrane, mechanically gated ion channel
110
What is the spatial connection between proteins DHP and RyR?
These 2 proteins are physically connected to each other, when not excited DHP in resting state and RyR is closed
111
When an action potential is fored down t-tubules, what happens that DHP and RyR facilitate?
DHP will change shape due to voltage change, tugs on connection with RyR receptor (trap door of sorts) calcium can then leave down the concentration gradient into ICFluid
112
Where else do we find nicotinic ACh receptors?
In the autonomic nervous system, in the post synaptic (ganglionic) cells of both branches, sympathetic and parasympathetic.
113
What will happen to the membrane potential when nAChRs open and why?
Permeability to both Na+ and K+ will increase, but we would expect depolarization of the membrane potential. This is because sodium will be entering the cell faster than K+ will leave the cell. This is because the electrochemical gradient is stronger for Na+ going into the cell than the one acting on K+.
114
Exposing myosin binding sites-
Without Ca2+ what happen?
Tropomyosin covers myosin binding sites on actin, no cross bridges (myosin heads) can bind to actin, muscle is relaxed.
115
Exposing myosin binding sites-
With Ca2+ what happen?
Ca2+ binds to troponin, tropomyosin moves away from myosin binding sites, cross bridges bind to actin, muscle contracts
116
More info about when calcium is there-
-myosin heads can grab onto actin (that’s the bridge between excitation and contraction)
(proteins have particular shape)
When calcium there, troponin will have shape change which will allow tropomyosin to move
117
Sliding filament mechanism-
During contraction, myofilaments slide past each other, shortening sarcomere
118
At rest is there much interaction between the thick and thin filaments?
Nope, at rest not much interaction or spatial closeness between thick and thin
119
Why does muscular contraction occur, and what are the thick and thin filaments doing to each other?
-during contraction 2 ends close to each other, causing more overlap between thin and thick, movement of thin filaments allows for all of this
-happens due to molecular interactions
120
Cross bridge cycle-
1) Binding of myosin to actin
(Hinge region between head and tail to head can pivot back and forth) grabbing actin in cocked position
121
Cross bridge cycle-
2) Power stroke
Myosin head moving from cocked to relaxed position, pulls thin filaments in direction of power stroke
122
Cross bridge cycle-
3) Detachment
&
4) Recocking
Myosin head lets go and then recocks and binds again (process just occurs over and over, thin filaments are getting pulled inward sorta) sarcomere gets shorter and muscle contracts
123
Cross bridge cycle-
As the cycle continues...
Sarcomere shortens
(two ends will continuously get closer, sarcomere getting shorter)
124
Cross bridge cycle:
overview
1) Binding of myosin to actin
2) Power stroke
3) Detachment
4) Re-cocking
As cycle continues, sarcomere shortens
125
Are myosin heads in synchrony with each other?
No
126
Cross Bridge cycle (simplified):
1) ATP hydrolysis “cocks” myosin
2) Actin-myosin bonds form, initiating power stroke
3) Pi released from myosin during power stroke
4) ADP released from myosin after power stroke
“Rigor” state
5) ATP binds to myosin, breaking bond with actin
127
Cross bridge cycle-
1) ATP hydrolysis “cocks” myosin
(if muscle not contracting this is the resting state, cant do anything bc tropomyosin covering binding sites on actin, once calcium comes in the cross bridge cycle can begin)
-once calcium comes in and exposes binding sites, myosin heads can bind actin, so the shape changes, causing power stroke, moving from cocked to relaxed position
-myosin ATPase
128
Cross bridge cycle-
2) actin-myosin bonds form
Initiation power stroke
ADP and inorganic phosphate have not left myosin head yet
129
Cross bridge cycle-
3) Pi released from myosin
during power stroke (as moves towards relaxed position)
130
Cross bridge cycle-
4) ADP released from myosin
after power stroke (“Rigor” state) myosin head relaxed still attached to actin,
131
Cross bridge cycle-
5) ATP binds to myosin, breaking bond with actin
Process can then restart
When power stoke has happened and ATPase is empty, there’s a tight bond between myosin and actin, doesn’t really mean anything bc about to be broken.
132
Cross bridge cycle-
5) ATP binds to myosin, breaking bond with actin
why result in rigor mortis?
When power stoke has happened and ATPase is empty, there’s a tight bond between myosin and actin, doesn’t really mean anything bc about to be broken.
But after death, no more ATP so myosin heads end up bound to actin in relaxed state, cause of rigor mortis
133
(Relaxation)
Sarcomere lengthens due to _______________________
(Muscle relaxation-
part e)
elastic properties
(elastic proteins within are real springy and just compress back, once myosin lets go of actin they stretch back out so thin filaments are back to where they were before.)
**see slides figure here 08 16
134
Muscle relaxation-
part a
Removing Ca2+ (first step muscle fiber stops firing action potential, so CA2+ from SR stops)
Calcium then needs to be put back
135
Muscle relaxation-
part b
-Ca2+ pumped back into SR with Ca2+ ATPase against its concentration gradient
136
Muscle relaxation-
part c
Calcium pops off of troponin, tropomyosin slides back so actin and myosin cant interact anymore
137
Muscle relaxation-
part d
-Tropomyosin covers myosin binding sites as Ca2+ removed from troponin
138
Excitation-contraction-
Timing of 2 events, what are?
Electrical events
&
Mechanical events
139
Timing of events-
Electrical events:
starts with action potential in motor neuron, results in neurotransmitter release at junction, then muscle fiber fires action potential
140
Timing of events-
Mechanical events:
Twitch- single cycle of contraction-relaxation
2 phases, contraction phase shorter sarcomeres, and then relaxation phase where calcium pumped back. Reduces force being produced
-as myosin grabs actin and pulls, generates force, as lets go, the force is being released
141
Altering the strength of contraction-
-Changing the number of contracting fibers (Recruitment)
-Change the stimulation frequency
(Summation, Tetanus)
-Changing the fiber length
142
Motor unit:
(recruitment)
A motor neuron and all the muscle fibers it controls (can have different numbers of muscle fibers and thus different amounts of force produced)
143
Recruitment-
activating more motor units to increase contraction
144
Summation-
-two twitches “piggyback” and add together
-occurs when muscle stimulated during contraction
-combined tension greater than individual twitch
-action potential fired before other finishes, so then builds
-releasing additional calcium opening up more binding sites for a stronger contraction
145
Tetanus-
-Maximum sustained contraction when stimulate muscle fiber for long period of time
-Producing a bunch of action potentials, some cause additional forces to be produced until maximum force is achieved
146
Fiber length-
-length-tension relationship
-maximum tension produced at optimal length, maximum cross bridge binding
147
Why does muscle length generally alter force output?
-tension decreases above and below optimal length
At resting muscle length, contraction with stimulation will be at maximum force, will be less if stretched, if it’s squished amount of force will be less. As you change length strength changes because amount of overlap of thin and thick filaments is changing
148
Why can a squished muscle not produce as much force?
-Overlap not as good when muscle stretched out, also not as good faster when squish (think about tug of war)
149
Why would a genetic mutation to the troponin gene disrupt muscle contraction?
The muscle would be unable to contract because you wouldn’t get calcium binding to the troponin, or when calcium binds it won’t result in tropomyosin to shift over, so the binding sites would be continually covered up.
150
With this mutation, would the myosin heads be cocked or relaxed, and what would be attached to the myosin ATPase?
The myosin heads would likely be cocked since the muscle is relaxed, and ADP and inorganic phosphate would be attached to the myosin ATPase, since this is after ATP hydrolysis.
151
Are the myosin heads cocked or relaxed, and attached or unattached to actin when ATP is bound to them?
The myosin heads would likely be relaxed with ATP bound, and they will be unattached to actin, and ATP hasn’t been hydrolyzed
152
In a hormonal pathway, "primary pathology" refers to a disorder originating within
the target endocrine gland itself
153
"secondary pathology" indicates a problem arising from
the pituitary gland
